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Biomedical subjects

M A Nathan

Publications and source records attributed to M A Nathan.

33 records · Page 2Linked to original sources
PubMed1977

Chronic labile hypertension produced by lesions of the nucleus tractus solitarii in the cat.

Bilateral electrolytic lesions of the nucleus tractus solitarii (NTS) were made at the level of the obex in seven cats. Within 1 hour the mean arterial pressure (MAP) rose to a maximum of 144 mm Hg (141% of control), and by 7 hours heart rate reached a peak of 236 beats/min (148% of control). The baroreceptor reflexes were abolished. After 24 hours the arterial pressure became extremely labile, with variations of 80-100 mm Hg observed. The lability occurred spontaneously and during behaviors that were self-initiated or elicited by environmental stimuli. The MAP in the lesion group was 144 mm Hg (180% of control) during the day, and 96 mm Hg (120% of control) at night. The lability, measured by the standard deviation, during the day in the lesion group was 4 times greater than in the control group and at night there were no differences. The heart rate of the lesion group was always higher than that of the control group but the lability of both groups was the same. We conclude that lesions of the NTS produced labile hypertension, probably by disinhibition of sympathetic activity through central interruption of the baroreceptor reflexes. The higher, more labile arterial pressures during the day may be caused by uninhibited increases in sympathetic activity elicited by environmental stimuli that are present during the day and absent at night. The daily variation of pressure may also be caused by somatomotor activity or by a daily rhythm of sympathetic activity which is unmasked by the lesions.

Acute Disease↗
PubMed1975

Fulminating arterial hypertension with pulmonary edema from release of adrenomedullary catecholamines after lesions of the anterior hypothalamus in the rat.

Bilateral electrolytic lesions of the anterior hypothalamus in unrestrained rats resulted in the development, within 2 hours, of arterial hypertension, tachycardia, hyperthermia, and increased locomotor activity, often leading to pulmonary edema and death. Similar lesions in paralyzed, artificially ventilated rats produced comparable changes in arterial blood pressure and body temperature with a similar time course. The arterial hypertension was a consequence of an increase in total peripheral resistance to 15% of control with a reduction in cardiac output to 49% of control. Arterial hypertension, elevated peripheral resistance, and diminished cardiac output were reversed toward normal by alpha-receptor blockade with phentolamine (1 mg/kg, iv). Bilateral adrenalectomy, adrenal demedullation, or adrenal denervation performed prior to lesion placement prevented the development of arterial hypertension and pulmonary edema as well as the changes in peripheral resistance, cardiac output, and body temperature. We conclude that arterial hypertension following lesions of the anterior hypothalamus is due to a neurally mediated increase in peripheral resistance initiated by the release of adrenal medullary catecholamines and that pulmonary edema is due to myocardial failure secondary to the ensuing ventricular overload. Structures originating in or passing through the anterior hypothalamus may exert selective control over the adrenal medulla independent of vasomotor neurons.

Adrenal Medulla↗
PubMed1973

Predatory attack, grooming, and consummatory behaviors evoked by electrical stimulation of cat cerebellar nuclei.

Electrical stimulation at single sites in the rostral fastigial nucleus elicits hypertension, grooming, feeding, and attack behaviors in the cat. The stimulus intensity and availability of suitable goal objects determines the behavior. Bilateral lesions of the area fail to produce motor deficits. The rostral fastigial nucleus may be a cerebellar area for behavioral and autonomic regulation.

Aggression↗
PubMed1968

Differential conditional emotional and cardiovascular responses--a training technique for monkeys.

A training technique has been developed which combines classical differential conditioning and conditional emotional response (CER) procedures. After monkeys were trained to lever-press on a variable-interval schedule, two stimulus lights were presented. One light (CS) was always followed, upon termination, by electrical shock; the other light (DS) was never followed by shock. The response to the CS was a decreased rate of lever-pressing and increased heart rate and blood-flow velocity. None of these responses occurred to the DS. This technique eliminates the possibility of pseudoconditioning and provides measurement of both somatic and autonomic responses in a CER situation.

Animals↗
PubMedDate not supplied

Pressor systems involved in the maintenance of arterial pressure after lesions of the rostral ventrolateral medulla.

The current study examined three pressor systems which might support mean arterial pressure (MAP) after lesions of the rostral ventrolateral medulla (RVLM). In two protocols, bilateral electrolytic lesions or sham lesions were placed in the RVLM of rats anesthetized with sodium pentobarbital. In the first protocol, the following drugs were given sequentially after placement of the lesions: captopril (5 mg/kg) and d-pentamethylene methylated tyrosine (30 micrograms/kg), a vascular arginine-vasopressin antagonist (AVPX). A final procedure consisted of spinal-cord transection. The second protocol was identical to the first except that the order of drug administration was reversed. In the first protocol, RVLM lesions caused a slight, but statistically significant, decrease in MAP from 118 +/- 3 mmHg to 103 +/- 5 mmHg. After captopril and AVPX, MAP further decreased to 87 +/- 5 mmHg and 62 +/- 4 mmHg, respectively. The MAP fell to 38 +/- 2 mmHg after spinal-cord transection. In the sham-lesion group, MAP rose slightly from 127 +/- 6 mmHg to 134 +/- 7 mmHg after placement of the sham lesions. A significant reduction in MAP was not seen until after administration of AVPX, which decreased MAP to 103 +/- 6 mmHg. Spinal-cord transection substantially lowered MAP to 36 +/- 4 mmHg. In the second protocol, RVLM lesions had no effect on MAP. Administration of AVPX had little effect on MAP (before: 117 +/- 5 mmHg; after: 102 +/- 7 mmHg). In contrast, sequential administration of captopril substantially decreased MAP to 55 +/- 5 mmHg. Spinal cord transection lowered MAP to 33 +/- 1 mmHg. A decrease in MAP in the companion sham-lesion group was not seen until after administration of captopril (before: 109 +/- 8 mmHg; after: 89 +/- 11 mmHg). The greatest fall in MAP followed spinal cord transection (to 39 +/- 6 mmHg). These results demonstrate normotension after RVLM lesions despite a marked reduction in sympathetic vasomotor activity. They also indicate that, after RVLM lesions, arterial pressure is maintained mainly by activity of the renin-angiotensin system and by AVP secretion.

Animals↗